States of shock, whatever their origin (cardiogenic, hemorrhagic and/or septic), lead to a drop in tissue perfusion with a more or less marked effect on small vessel perfusion. This microcirculatory impairment leads to a dysfunction or even failure of various organs, which worsens patient prognosis. Currently, there is a need for monitors capable of reflecting the microcirculatory perfusion state. Among the instruments recently developed, some monitors measure tissue CO2 and perfusion index (or PI).
The measurement of the partial CO2 pressure in tissues (PtissueCO2) has been identified as a reliable marker of tissue perfusion in many publications: an increase in tissue CO2, in particular compared with arterial CO2 (calculation of the tissue-arterial gradient: Pt−aCO2), reflects tissue accumulation of CO2 due to a concomitant drop in perfusion. The devices currently available for measuring tissue CO2 are gastric tonometry (PgCO2) or sublingual measurement (PslCO2). Recently, the measurement of cutaneous CO2 (PcCO2) at the earlobe has been described as a measurement of tissue CO2 (WO 2011/024018). Like the other measurements of tissue CO2, an elevation in cutaneous CO2 at the earlobe is a marker for poor prognosis in states of shock and a reliable reflection of microcirculatory perfusion.
The perfusion index (PI), derived from the oxygen saturation (SpO2) plethysmography signal, reflects the pulsatile part of the SpO2 signal. This parameter and especially variations therein during the treatment of patients have been described as a reliable reflection of tissue perfusion.
However, the diagnosis of an impairment of microcirculatory perfusion during a state of shock does not make it possible to guide the therapy since these impairments can have various etiologies and therefore require very diverse therapies. Two situations may schematically be encountered:    (1) “Predominant central” problem: due to a generalized hypoperfusion owing to a low cardiac output leading to a macrocirculatory hypoperfusion and therefore also a microcirculatory hypoperfusion (situation encountered in the acute phase of a state of hemorrhagic or cardiogenic shock). In this situation, there is usually no damage to the integrity of the endothelial and microcirculatory function, the peripheral hypoperfusion is due to a drop in overall perfusion. After restoration of central hemodynamics, the microcirculatory hypoperfusion may either rapidly return to normal, or decrease without completely returning to normal due to vasoconstriction of the peripheral territories (such as the skin) favoring perfusion of the noble organs. This case corresponds to a “distributive” problem, due to the abnormality of redistribution from the central blood flow to regional flows, which leads to a residual peripheral hypoperfusion but without structural abnormality of the microvessels and of the endothelial function.    (2) “Predominant peripheral” problem: due to a functional impairment of the state of the microvessels with vascular rarefaction and destruction of the integrity of the vascular endothelium, leading to an abolition of reactional vasodilation and creating a real obstacle to tissue perfusion without any adaptive possibility. In this case, little or no central hypoperfusion is observed, but a direct effect on microcirculatory function, leading to peripheral hypoperfusion, is observed. This situation is encountered in cases of septic shock after initial hemodynamic treatment, but also in various pathological conditions where affected vascular reactivity and affected microcirculation are frequent and influence patient prognosis (for example in the case of diabetic patients, of patients with chronic hypertension, of patients suffering from system disease with angiitis, of patients suffering from renal failure, etc.).
These two situations can give the same quantitative evaluation of the impairment of microcirculatory perfusion (same elevation of tissue CO2 and same decrease in PI), although they require fundamentally different therapies. In situation (1), termed “predominant central”, an attempt will be made to rapidly restore central hemodynamics in a long-lasting manner, which will lead to a gradual improvement in microcirculatory perfusion. In situation (2), termed “predominant peripheral”, the prognosis is more serious because of the structural damage to the microcirculation; etiological treatment is predominant and therapies specific to this situation are still currently being studied.